Intercellular adhesion molecule-1(ICAM-a)is an important molecule in mediating immune and inflammatory responses. It is found on the surface of hematopoietic and nonhematopoietic cells. It can act as an adhesive ligand for integrins such as
LFA-1(Cd18/CD11a) and MAC-1(Cd18/CD11b). ICAM-1 is basally expressed in significant amount on a limited number of cell types, including monocytes and endothelialcells. But it is inducible or upregulated by INF-γ, IL-1β and TNF-α onmany cell
types.
IL-4, a pleiotropic cytokine and mast cell differentiation factor, is upregulated in human allergic disease and stimulates expression of vascular adhesion molecule-1(VCAM-1) in endothelial cells. IL-4 also promotes expression of surface ICAM-1 in
human
mast cells and dermal fibroblasts. So in allergic rhinitis and asthma, IL-4 maybe an important cytokine implicated in the pathogenesis of inflammation. We studied the effect of INF-γ and IL-4 on expression of ICAM-1 in human nasal epithelial
cells)HNEC). HNEC were prepared by primary culture method of monolayer culture of dissociated cells from human inferior nasal turbinate mucosa. Nasal mucosa were obtained by partial turbinectomy of septal deviation patients. Primary cultured
cells
were
charaterized as an epithelial cell type by indirect immunofluorescence assay using antibodies against cytokeratin-pan, cytokeratin No. 8, vimentin and von Willebrand factor. Using fluorescence activated cell sorter(Coulter ELITE), we analyzed the
quantitative expression of ICAM-1 on HNEC. Treatment of HNEc with IFN-γ(1ng/ml) for 24 hours caused about 8 fold increase of the surface ICAM-1 compared with constitutive expression by mean fluorescence intensity (MIF) but IL-4 had little
effect.
Theses foundings suggest that IFN-γis a potent ICAM-1 inducer in HNEC and further studies are necessary for the role of IL-4 on HNEC.
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